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MSK II Exam I > Intro to pharm > Flashcards

Intro to pharm Flashcards

1
Q

Antibacterial Agents

A

Bacitracin and gramicidin
Mupirocin
Polymyxin B sulfate
Neomycin and gentamicin

Topical antibiotics in acne: 
Clindamycin (Cleocin)  
Erythromycin (Erygel)
Metronidazole (Metrogel)
Sodium sulfacetamide
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2
Q

Topical Antiviral Agents

A

Acyclovir, penciclovir, docosanol (Abreva)

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3
Q

Topical antifungal preparations

A 
Azoles – clotrimazole
miconazole 
ketoconazole, 
Ciclopirox olamine 
Allylamines – terbinafine 
Butenafine
Tolnaftate 
Nystatin and amphotericin B
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4
Q

Oral antifungal agents

A

Azoles – ketoconazole, itraconazole, fluconazole, voriconazole

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5
Q

Immunomodulators

A

Imiquimod

Tacrolimus and pimecrolimus

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6
Q

Acne Preparations

A

Retinoic acid and derivatives: retinoic acid (tretinoin), adapalene ,
tazarotene
Isotretinoin
Benzoyl peroxide

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7
Q

Drugs for Psoriasis

A

Acitretin
Tazarotene
Calcipotriene
Cyclosporine

Biologic response modifiers
TNF inhibitors – etanercept
infliximab , adalimumab

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8
Q

Anti-Inflammatory Agents

A

Topical corticosteroids

Examples include hydrocortisone, hydrocortisone valerate, triamcinolone acetonide, betamethasone

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9
Q

Keratolytic and Destructive Agents

A

Salicylic acid

Fluorouracil

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10
Q

Antipruritic Agents

A

Antihistamines

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11
Q

Trichogenic and Antitrichogenic Agents

A

Minoxidil , finasteride

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12
Q

Skin function:

A 
Protection
Thermal regulation
Immune responsiveness
Biochemical synthesis
Sensory detection
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13
Q

Variables determining response

A

Drug penetration
Concentration gradient
Dosing schedule
Vehicles and occlusion

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14
Q

Drug Absorption

A

Three routes:

  • Intact stratum corneum
  • Sweat ducts
  • Sebaceous follicles

Steps involved in percutaneous absorption:

  • Concentration gradient established
  • Partition coefficient
  • Diffusion coefficient

Rate of absorption:
J = Cveh · Km · D/x

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15
Q

drying preparations to lubricating preparations

A

tinctures < wet dressings < lotions < gels < aerosols < powders < pastes < creams < ointments

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16
Q

what do we use for Chronic inflammation with xerosis, scaling, lichenification

A

creams and ointments

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17
Q

what do we use for Acute inflammation with oozing, vesiculation, and crusting

A

tinctures, wet dressings, and lotions

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18
Q

Transdermal Patches

A 
fentanyl for pain
lidocaine for neuralgia 
ethinyl estradiol/ norelgestromin for contraception
nitroglycerin for angina
scopolaine for motion sickness
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19
Q

general treatment approach for abrasions

A

clean minor injuries (scratches, cuts, abrasions) with soap and water
use of topical abx is mixed– worry about skin sensitivity/ promotion of resistance
clean wounds and remove debris

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20
Q

What are the mechanisms of action of the individual components of Neosporin (bacitracin, neomycin, polymyxin B)?

A. Increases permeability of cell wall
B. Inhibits cell wall synthesis
C. Inhibits 30S ribosomal subunit

A

polymixin B- increases permeability of cell wall
bacitracin- inhibits cell wall synthesis
neomycin- inhibits 30S ribosomal subunit

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21
Q

A 5 yo female is brought to urgent care by her mother after returning from kindergarten with red sores around her mouth.
You suspect non-bullous impetigo and would like to suggest a topical antibiotic ointment.
Which two topical antimicrobials cover group A β-hemolytic streptococci and S. aureus (including MRSA)?
Mupirocin
Neomycin
Polymyxin B
Retapamulin

A

neomycin and polymyxin B are not good for gram positive organisms.

Use mupirocin and retapamulin

mupirocin has good in vitro activity against MRSA but there’s no good clinical evidence

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22
Q

kid with non-bullous impetigo. General treatment approach

A

non-bullous impetigo- topical therapy with mupirocin or retapamulin for 5 days

more extensive forms of impetigo and bullous forms- oral abx for 7 days

Benefits of topical therapy: fewer side effects, lower risk of bacterial resistance.

Bacitracin-neomycin-polymixin B has some activity against impetigo causing organisms, but- may be less effective, and bacitracin and neomycin can cause contact dermatitis

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23
Q

Topical Antibiotics in Acne

A

Avoid systemic exposure and achieve high follicular concentrations
Less effective than systemic administration of the same antibiotic
Available options:
- Clindamycin
- Erythromycin
- Metronidazole
- Sodium sulfacetamide

Not used as monotherapy (bacterial resistance)!
- Give with benzoyl peroxide or retinoids

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24
Q

Clindamycin MOA

A

inhibits 50s ribosomal subunit

25
erythromycin MOA
inhibits 50s ribosomal subunnit
26
metronidazole MOA
damages DNA
27
sodium sulfacetamide MOA
inhibits folic acid synthesis
28
increased sebum production in acne creates a lipi rich microaerobic environment favorable to what organism?
propionibacterium acnes
29
A 35 yo male construction worker presents to his PCP with complaints of intense itching of both feet throughout the day. PE: webs spaces white, macerated, cracked Workup consistent with dermatophyte infection What topical therapeutic options are available?
azoles, allylamine, butenafine, tolnaftate pt/ provider preference, etc.
30
topical Azoles – clotrimazole, miconazole | MOA, uses
MOA: inhibits synthesis of ergosterol (inhibits lanosterol 14-α-demethylase) Uses: tinea corporis (ring worm), tinea pedis (athlete’s foot), tinea cruris (jock itch), tinea versicolor, and cutaneous candidiasis, such as vaginal yeast infections, infections of the skin, diaper rash, and thrush (candidiasis of the oral mucosa and tongue, and sometimes the palate, gingivae, and floor of the mouth)
31
topical Ciclopirox olamine | MOA, uses
MOA: inhibits uptake of precursors of macromolecule synthesis Uses: topical dermatomycosis, candidiasis, tinea versicolor, mild-to-moderate onychomycosis
32
topical Allylamines – terbinafine and naftifine | MOA, uses
MOA: inhibits squalene epoxidase Uses: tinea corporis, tinea cruris, and tinea pedis
33
topical tolnaftate MOA, uses
MOA unknown. | Uses: tinea pedis, tinea cruris, and tinea corporis
34
topical Nystatin/amphotericin B MOA, uses
MOA: binds ergosterol in fungal cell membrane altering permeability Nystatin limited to topical cutaneous and mucosal uses - Thrush Amphotericin B broad antifungal spectrum but rarely used topically Cumulative organ toxicity “ampho-terrible”
35
oral azoles: uses
Uses: vaginal, urinary, oropharyngeal, or esophageal candida infections Systemic yeast infections more common: type 1 diabetes, leukemia, AIDS Drug-drug interactions!
36
oral griseofulvin: MOA, uses
MOA: inhibits fungal cell mitosis at metaphase Uses: dermatophyte infections but not Candida Induces CYP enzymes
37
oral terbinafine: uses
High first pass metabolism; accumulates in skin, nails, fat | Uses: tinea corporis, tinea capitis, and onychomycosis
38
Antifungal Agents for dermatophyte infections- by location
``` Tinea capitis (scalp) – oral griseofulvin, terbinafine, itraconazole Tinea pedis (feet) – topical antifungals Tinea cruris (groin) – topical antifungals Tinea corporis (body) – topical antifungals, oral antifungals ```
39
antifungal agents for candida
Thrush (oropharyngeal candidiasis) – oral nystatin, clotrimazole troche, oral fluconazole Esophageal candidiasis – systemic antifungals Vulvovaginitis – topical antifungals, oral fluconazole Invasive infection – systemic antifungals
40
A 40 yo male seeks your recommendation regarding frequent cold sores. He experiences about ten cold sores a year, exacerbated by “colds” or sun exposure. What organism is causing these cold sores? He wants to know what treatment options are available to him.
Herpes simplex topical acyclovir, penciclovir, or docosonol- modest benefit apply within 1 hour of first sign or symptom, continue x 4 days oral acyclovir, famcyclovir, valacyclovir- begin within 1 hour chronic suppressive therapy for > 6 recurrences per year (acyclovir, valacyclovir)
41
Acyclovir, valacyclovir, penciclovir, famciclovir | MOA, uses
MOA: converted to pharmacologically active triphosphate metabolites, inhibit DNA synthesis and viral replication Topical – modest benefit for herpes labialis Systemic – Most effective in treating herpes labialis Also used systemically for HSV and VZV infections
42
Docosanol | MOA and uses
MOA: inhibits fusion between the plasma membrane and the HSV envelope, thereby preventing viral entry and replication When applied within 12 hours of the onset of prodromal symptoms, five times daily, median healing time was shortened by 18 hours compared with placebo in recurrent orolabial herpes
43
Imiquimod | MOA, uses, ADRs
MOA: may be related to stimulation of peripheral mononuclear cells to release interferon-α and macrophage stimulation to produce interleukins-1, -6, -8, and TNF-α Uses: external genital and perianal warts in adults, actinic keratoses on the face and scalp, biopsy-proven primary basal cell carcinomas on the trunk, neck, and extremities (< 2 cm diameter) ADRs: local inflammation, pruritus, erythema, superficial erosion
44
Tacrolimus | MOA, uses, ADRs
MOA: inhibit T-lymphocyte activation and prevent release of inflammatory cytokines and mediators from mast cells Uses: treatment of atopic dermatitis and psoriasis but traditionally used to prevent heart, liver, and kidney allograft rejection due to potent immunosuppressive activity (oral forms) Topical ADRs: transient erythema, burning, and pruritus
45
What is the mechanism of action of benzoyl peroxide?
releases free-radical oxygen which oxidizes bacterial proteins, activity against P. acnes (no resistance)
46
14 y/o with mild acne. Other treatment options besides benzoyl peroxide?
topical retinoids: tretinoin (all-trans-retinoic acid)- also marketed as anti-aging adapalene- photo-chemically more stable, less irritating tazarotene-- also approved for psoriasis, photoaging MOA- may decrease cohesion between epidermal cells and increase epidermal cell turnover, expulsion of open comedones adn the transformation of closed comedones into open ADRs: erythema, mild peeling and dryness; minimize sun exposure CI: not recommended in pregnant women
47
Severe Cystic Acne- treatment
Isotretinoin (PO) MOA: reduces sebacerous gland size, reduces sebum production PK: t1/2 10-20 hours; hepatic metabolism; highly protein bound (99-100%) ADRs: resemble hypervitaminosis A (dryness and itching) Must pledge to be on 2 contraceptives and take pregnancy tests
48
Acne Treatment Approach
Comedonal (non-inflammatory) acne - Topical retinoid - - Alternatives: azelaic acid, salicylic acid Mild papulopustular and mixed acne - Topical retinoid AND topical antimicrobial (BPO alone or BPO +/- topical antibiotic) Moderate papulopustular and mixed acne - Topical retinoid AND oral antibiotic AND topical BPO Moderate nodular acne - Topical retinoid AND oral antibiotic AND topical BPO Severe nodular/conglobate acne - Oral isotretinoin
49
Psoriasis topical therapy
Emollients – used as basic adjunct; reduces scaling, itching, and related discomfort Keratolytics – reduce hyperkeratosis; enable other topical drugs to penetrate Topical glucocorticoids – rapid response; control inflammation and itching; mainstay of topical treatment 2nd line alternatives: Coal tar Anthralin – used for widespread, refractory plaques Calcipotriene – as effective as topical glucocorticoids but slower onset; no long-term glucocorticoid adverse effects Tazarotene – extended response; maintenance therapy
50
Psoriasis systemic therapy
Used for patients with > 5% body surface area involvement Methotrexate - MOA: inhibits dihydrofolate reductase (folic acid analog) - Used in combination with phototherapy or biological agents - Effective for both skin lesions and arthritis Acitretin - Systemic retinoic acid derivative - Not as effective as other systemic therapies Cyclosporine - MOA: inhibits calcineurin, inhibits transcription of interleukin-1 and -2 receptors, blocks T-cell activation - ADRs: nephrotoxicity, hypertension, hepatotoxicity, gingival hyperplasia, and hirsutism - Used in extensive disease in patients who are unresponsive to other agents
51
Psoriasis- Biologic Response Modifiers
Tumor necrosis factor inhibitors (etanercept, infliximab, adalimumab) - MOA: prevents TNF mediated immune responses - ADRs: risk of serious life-threatening infections (sepsis, pneumonia), exacerbation of congestive heart failure, and cause demyelinating disease in predisposed patients - What infectious disease must be ruled out before initiating therapy with TNF inhibitors? TB
52
Topical Corticosteroids
Immunosuppressive and anti-inflammatory Local (topical & intralesional) or systemic (IM, IV, PO) - Systemic therapy reserved for severe dermatological illness (allergic contact dermatitis to plants, life-threatening vesiculobullous dermatoses) Corticosteroids are minimally absorbed following application to normal skin
53
Regional variation of percutaneous corticosteroid absorption
``` feet-- terrible palm forearm scalp- getting better forehead genitalia- most ```
54
Topical Corticosteroids | - groupings
Grouped into classes based on potency or approximate relative efficacy Low to medium efficacy produce remission in disorders responsive to corticosteroids: seborrheic dermatitis, psoriasis of genitalia and face High efficacy preparations useful in disorder less responsive to corticosteroids: psoriasis of palms and soles, sarcoidosis ADRs: suppression of pituitary-adrenal axis - Atrophy, steroid rosacea, steroid acne, allergic contact dermatitis
55
lowest to highest efficacy of topical corticosteroids
``` hydrocortisone betamethasone valerate hydrocortisone valerate betamehasone dipropionate Clobetasol propionate ```
56
Keratolytic Agents
Keratolytic: peeling agent causing softening/dissolution or peeling of stratum corneum Salicylic acid Uses: acne, seborrheic dermatitis, psoriasis, hyperkeratosis (corns, plantar warts, calluses); in combination with antifungal sodium thiosulfate for tinea versicolor Salicylate toxicity can occur (nausea, vomiting, dizziness, loss of hearing, tinnitus, lethargy, diarrhea, psychic disturbances)
57
AntiPruritic Agents
Corticosteroids, local anesthetics Topical therapy useful in localized pruritus Systemic therapy generally used for generalized pruritus Antihistamines First generation H1-receptor antagonists - Diphenhydramine, promethazine - Some anticholinergic activity, sedating, useful in nocturnal pruritus Second generation H1-receptor antagonists - Cetirizine, loratadine, desloratadine, fexofenadine - Do no cross blood-brain barrier, lack anticholinergic side effects, non-sedatin
58
Trichogenic Agents
Trichogen: agent that promotes hair growth Minoxidil MOA: unknown - Originally developed as an antihypertensive (PO dosing) - Percutaneous absorption minimal but systemic effects on BP should be monitored in those with cardiac disease Finasteride - MOA: competitive and selective inhibitor of steroid 5α-reductase; blocks the conversion of testosterone to dihydrotestosterone (DHT) - ADRs: decreased libido, ejaculation disorders, erectile dysfunction - Pregnant women should not handle drug

MSK II Exam I (16 decks)

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